Epstein–Barr virus: more than 50 years old and still providing surprises

Abstract

It is more than 50 years since the Epstein-Barr virus (EBV), the first human tumour virus, was discovered. EBV has subsequently been found to be associated with a diverse range of tumours of both lymphoid and epithelial origin. Progress in the molecular analysis of EBV has revealed fundamental mechanisms of more general relevance to the oncogenic process. This Timeline article highlights key milestones in the 50-year history of EBV and discusses how this virus provides a paradigm for exploiting insights at the molecular level in the diagnosis, treatment and prevention of cancer.

LTRs activated by Epstein-Barr virus-induced transformation of B cells alter the transcriptome

“…The activation of these two genes, however, may have, in the long run, negative consequences for the host in the form of the oncogenesis. EBV has long been associated with increased risk of lymphoma (Young et al 2016). Interestingly, analysis of lymphoma cell transcriptomes revealed many TE-driven chimeric transcripts (Lock et al 2014;).…”

Higher incidence of nasopharyngeal carcinoma in some regions in the world confers for interplay between genetic factors and external stimuli

“…EBVs can persist latently in the B-cells for the lifetime of a person after initial infection. All latency programs may exist in B-cells and can move into lytic phase; eventually giving birth of infectious virions which may infect epithelial cells of the same or other person(s) depending upon the route of infection (65,66). After initial infection, the EBV nuclear antigens (EBNAs) are expressed along with some cellular proteins.…”

Exosomes as the Promising Biomarker for Epstein-Barr Virus (EBV)-Associated Cancers

“…For instances, LMP1, which is a viral mimic of tumour necrosis factor receptor (TNFR) family member CD40, has been reported to activate a cascade of oncogenic signalling pathways such as nuclear factor kappa B (NF-κB), phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and c-Jun N-terminal kinases (JNKs) in EBV-associated cancers [10,16,17]. On the other hand, LMP2 plays central roles in maintaining viral latency in EBV-infected B cells as well as inducing transformation and migration of EBV-infected cells [10,16,17]. Whether or not the functions of cell-associated LMPs are fully retained in the exosomal LMPs, it remains to be proven.…”